Books: 'Mammalian tissues'

1

Electrical properties of mammalian tissues: An introduction. London: Chapman & Hall, 1992.

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2

He, Juan. Theophylline 7-[beta]-D ribofuranoside production in mammalian tissues. Ottawa: National Library of Canada, 1994.

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3

1942-, Harris Stephen E., and Mansson Per-Erik, eds. Cellular factors in development and differentiation: Embryos, teratocarcinomas, and differentiated tissues : proceedings of the Third International Symposium on Cellular Endocrinology, held at Lake Placid, New York, August 30-September 2, 1987. New York: Liss, 1988.

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4

The cellular structure of the mammalian nervous system: A re-examination, and some consequences for neurobiology. Lancaster: MTP Press, 1986.

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5

Glutamine Metabolism in Mammalian Tissues. Springer, 2011.

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6

Sies, H., and D. Häussinger. Glutamine Metabolism in Mammalian Tissues. Springer London, Limited, 2012.

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7

Sies, H., and D. Häussinger. Glutamine Metabolism in Mammalian Tissues. Springer, 2011.

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8

He, Juan. Theophylline 7-B-D ribofuranoside production in mammalian tissues. 1995.

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9

Symonds, Michael E., and Rafael Franco, eds. Epigenetics Traits in Mammalian Tissues. From New Technology to New Hypotheses. Frontiers Media SA, 2019. http://dx.doi.org/10.3389/978-2-88963-037-0.

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10

Cellular factors in development and differentiation: Embryos, teratocarcinomas, and differentiated tissues : Proceedings of the Third International Symposium ... in clinical and biological research). Liss, 1988.

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11

Girardier, Lucien. Mammalian Thermogenesis. Springer London, Limited, 2012.

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12

Guckenburg, William J. Mammalian cell cultivations. 1990.

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13

1945-, Gash Don M., Sladek John R, American Paralysis Association, and Schmitt Symposium on Transplantation into the Mammalian Central Nervous System (1987 : Rochester, N.Y.), eds. Transplantation into the mammalian CNS. Amsterdam: Elsevier, 1988.

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14

Burton, Derek, and Margaret Burton. Metabolism, homeostasis and growth. Oxford University Press, 2017. http://dx.doi.org/10.1093/oso/9780198785552.003.0007.

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Metabolism consists of the sum of anabolism (construction) and catabolism (destruction) with the release of energy, and achieving a fairly constant internal environment (homeostasis). The aquatic external environment favours differences from mammalian pathways of excretion and requires osmoregulatory adjustments for fresh water and seawater though some taxa, notably marine elasmobranchs, avoid osmoregulatory problems by retaining osmotically active substances such as urea, and molecules protecting tissues from urea damage. Ion regulation may occur through chloride cells of the gills. Most fish are not temperature regulators but a few are regional heterotherms, conserving heat internally. The liver has many roles in metabolism, including in some fish the synthesis of antifreeze seasonally. Maturing females synthesize yolk proteins in the liver. Energy storage may include the liver and, surprisingly, white muscle. Fish growth can be indeterminate and highly variable, with very short (annual) life cycles or extremely long cycles with late and/or intermittent reproduction.

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15

Hope, James, and Mark P. Dagleish. Prion-protein-related diseases of animals and man. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0041.

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Scrapie, bovine spongiform encephalopathy (BSE), Creutzfeldt–Jakob disease (CJD), and related diseases of mink (transmissible mink encephalopathy), mule deer and elk (chronic wasting disease) are the founder members of a group of diseases called the transmissible degenerative (or spongiform) encephalopathies (TSE). These diseases can be transmitted by prions from affected to healthy animals by inoculation or by feeding diseased tissues. Prions are cellular proteins that can transfer metabolic and pathological phenotypes vertically from parent to progeny or horizontally between cells and animals. TSEs are characterised by the accumulation of the prion form of the mammalian prion protein (PrPC) in the central nervous system or peripheral tissues of animals and humans. Mutations of the human PrP gene are linked to rare, familial forms of disease and prion-protein gene polymorphisms in humans and other species are linked to survival time and disease characteristics in affected individuals. Iatrogenic transmission of CJD in man has occurred, and a variant form of CJD (vCJD) is due to cross-species transmission of BSE from cattle to humans. Atypical forms of scrapie and BSE have been identified during large-scale monitoring for TSEs worldwide. This chapter outlines our current understanding of scrapie, BSE, CJD and other TSEs and highlights recent progress in defining the role in disease of the prion protein, PrP.

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16

(Editor), Don M. Gash, Schmitt Symposium on Transplantation into the Mammalian Central nervou (Corporate Author), American Paralysis Association (Corporate Author), and John R., Jr. Sladek (Editor), eds. Transplantation in the Mammalian Cns (Progress in Brain Research). Elsevier Publishing Company, 1989.

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17

Peptides in Mammalian Protein Metabolism: Tissue Utilisation & Clinical Targetting (Portland Press Proceedings,). Ashgate Publishing, 1997.

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18

Naimark, Wendy Alison. Structure/function relations in mammalian pericardial tissue: Implications for comparative and developmental physiology. 1996.

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19

Lloyd, Sheelagh. Other adult and larval cestodes. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0059.

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Adult Diphyllobothrium latum is acquired by consumption of raw fish by persons living around lakes/reservoirs/rivers. Hymenolepis nana can have a direct life cycle so eggs produced by adults in man are important in transfer between humans. The contribution of rodents and the indirect life cycle through arthropods need re-evaluation. Other minor adult cestode infections are described.Man can be an intermediate host for tissue metacestodes. Taenia multiceps and related species are that acquired from canids and produce a coenurus. Spirometra spp. pleurocercoids are acquired from copepod or reptile/amphibian/mammalian intermediate hosts. Other metacestode infections are very rare.

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20

Hillman, Harold. Cellular Structure of the Mammalian Nervous System: A Re-Examination, and Some Consequences for Neurobiology. Springer, 2012.

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21

The Cellular Structure of the Mammalian Nervous System: A re-examination, and some consequences for neurobiology. Springer, 2012.

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22

Salvatori, Daniela, Harsha D. Devalla, and Robert Passier. Cells to repair the infarcted myocardium. Edited by José Maria Pérez-Pomares, Robert G. Kelly, Maurice van den Hoff, José Luis de la Pompa, David Sedmera, Cristina Basso, and Deborah Henderson. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198757269.003.0030.

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The adult mammalian heart has poor regenerative capacity. Loss of functional cardiomyocytes following myocardial infarction leads to the replacement of functional muscle by scar tissue. This has a detrimental effect on cardiac function and may lead to heart failure. Potential regeneration of severe cardiac damage would require replacement of dead and damaged cardiomyocytes by transplantation, recruitment of endogenous progenitor cells, or induction of cardiomyocyte proliferation. For more than a decade, clinical trials to ameliorate the injured heart have been under way. However, after evaluation of the outcome of these trials it is evident that the beneficial effects of these cell-based transplantations are only marginal, and beneficial effects, if any, are not caused by regeneration of cardiomyocytes. In recent years, alternative approaches and various cell sources have been studied and suggested for cardiac repair. Recent advances in these cell-based therapies or strategies to activate endogenous cardiac repair are discussed.

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23

Flanagan, Stuart. Pneumocystis jirovecii. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0019.

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In humans, Pneumocystis pneumonia is caused by a yeast-like fungus Pneumocystis jirovecii. Originally called P. carinii, this organism was thought to be a protozoan; however, the discovery of chitin, β‎-1,3-glucan, and ergosterol in the cell wall confirmed it as a fungus. DNA analysis demonstrated that the human disease was caused by P. jirovecii, while P. carinii was found to infect rats. P. jirovecii resides in mammalian lung tissue, usually without ill effects, but in immunocompromised hosts it becomes pathogenic and causes respiratory infection. P. jirovecii has been isolated from air and pond water samples; pond water is the potential source of infection. Almost 90% of cases of Pneumocystis pneumonia occur in HIV-positive individuals with CD4 T-cell counts below 200 cells per microlitre. The infection is diagnosed by clinical history, assessment of oxygenation levels, and direct microscopy of sputum or bronchoalveolar lavage samples. Treatment requires antibiotics and HAART (highly active antiretroviral therapy) for HIV infection.

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24

George, Grimble, and Backwell F. R. C, eds. Peptides in mammalian protein metabolism: Tissue utilization and clinical targeting : proceedings of the conference held at the Rowett Research Institute, Aberdeen, in September 1994. London: Portland, 1998.

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25

Kühn, Wolfgang, and Gerd Walz. The molecular basis of ciliopathies and cyst formation. Edited by Neil Turner. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0303.

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Abnormalities of the cilium, termed ‘ciliopathies’, are the prime suspect in the pathogenesis of renal cyst formation because the gene products of cystic disease-causing genes localize to them, or near them. However, we only partially understand how cilia maintain the geometry of kidney tubules, and how abnormal cilia lead to renal cysts, and the diverse range of diseases attributed to them. Some non-cystic diseases share pathology of the same structures. Although still incompletely understood, cilia appear to orient cells in response to extracellular cues to maintain the overall geometry of a tissue, thereby intersecting with the planar cell polarity (PCP) pathway and the actin cytoskeleton. The PCP pathway controls two morphogenetic programmes, oriented cell division (OCD) and convergent extension (CE) through cell intercalation that both seem to play a critical role in cyst formation. The two-hit theory of cystogenesis, by which loss of the second normal allele causes tubular epithelial cells to form kidney cysts, has been largely borne out. Additional hits and influences may better explain the rate of cyst formation and inter-individual differences in disease progression. Ciliary defects appear to converge on overlapping signalling modules, including mammalian target of rapamycin and cAMP pathways, which can be targeted to treat human cystic kidney disease irrespective of the underlying gene mutation.

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26

Roe, Simon, ed. Protein Purification Techniques. Oxford University Press, 2001. http://dx.doi.org/10.1093/oso/9780199636747.001.0001.

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Proteins are an integral part of molecular and cellular structure and function and are probably the most purified type of biological molecule. In order to elucidate the structure and function of any protein it is first necessary to purify it. Protein purification techniques have evolved over the past ten years with improvements in equipment control, automation, and separation materials, and the introduction of new techniques such as affinity membranes and expanded beds. These developments have reduced the workload involved in protein purification, but there is still a need to consider how unit operations linked together to form a purification strategy, which can be scaled up if necessary. The two Practical Approach books on protein purification have therefore been thoroughly updated and rewritten where necessary. The core of both books is the provision of detailed practical guidelines aimed particularly at laboratory scale purification. Information on scale-up considerations is given where appropriate. The books are not comprehensive but do cover the major laboratory techniques and common sources of protein. Protein Purification Techniques focuses on unit operations and analytical techniques. It starts with an overview of purification strategy and then covers initial extraction and clarification techniques. The rest of the book concentrates on different purification methods with the emphasis being on chromatography. The final chapter considers general scale-up considerations. Protein Purification Applications describes purification strategies from common sources: mammalian cell culture, microbial cell culture, milk, animal tissue, and plant tissue. It also includes chapters on purification of inclusion bodies, fusion proteins, and purification for crystallography. A purification strategy that can produce a highly pure single protein from a crude mixture of proteins, carbohydrates, lipids, and cell debris to is a work of art to be admired. These books (available individually or as a set)are designed to give the laboratory worker the information needed to undertake the challenge of designing such a strategy.

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27

Joyner, Alexandra, ed. Gene Targeting. Oxford University Press, 1999. http://dx.doi.org/10.1093/oso/9780199637928.001.0001.

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Since the publication of the first edition of Gene Targeting: A Practical Approach in 1993 there have been many advances in gene targeting and this new edition has been thoroughly updated and rewritten to include all the major new techniques. It provides not only tried-and-tested practical protocols but detailed guidance on their use and applications. As with the previous edition Gene Targeting: A Practical Approach 2e concentrates on gene targeting in mouse ES cells, but the techniques described can be easily adapted to applications in tissue culture including those for human cells. The first chapter covers the design of gene targeting vectors for mammalian cells and describes how to distinguish random integrations from homologous recombination. It is followed by a chapter on extending conventional gene targeting manipulations by using site-specific recombination using the Cre-loxP and Flp-FRT systems to produce 'clean' germline mutations and conditionally (in)activating genes. Chapter 3 describes methods for introducing DNA into ES cells for homologous recombination, selection and screening procedures for identifying and recovering targeted cell clones, and a simple method for establishing new ES cell lines. Chapter 4 discusses the pros and cons or aggregation versus blastocyst injection to create chimeras, focusing on the technical aspects of generating aggregation chimeras and then describes some of the uses of chimeras. The next topic covered is gene trap strategies; the structure, components, design, and modification of GT vectors, the various types of GT screens, and the molecular analysis of GT integrations. The final chapter explains the use of classical genetics in gene targeting and phenotype interpretation to create mutations and elucidate gene functions. Gene Targeting: A Practical Approach 2e will therefore be of great value to all researchers studying gene function.

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28

Grant, Warren, and Martin Scott-Brown. Principles of oncogenesis. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0322.

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It is obvious that the process of developing cancer—oncogenesis—is a multistep process. We know that smoking, obesity, and a family history are strong independent predictors of developing malignancy; yet, in clinics, we often see that some heavy smokers live into their nineties and that some people with close relatives affected by cancer spend many years worrying about a disease that, in the end, they never contract. For many centuries scientists have struggled to understand the process that make cancer cells different from normal cells. There were those in ancient times who believed that tumours were attributable to acts of the gods. Hippocrates suggested that cancer resulted from an imbalance between the black humour that came from the spleen, and the other three humours: blood, phlegm, and bile. It is only in the last 100 years that biologists have been able to characterize some of the pathways that lead to the uncontrolled replication seen in cancer, and subsequently examine exactly how these pathways evolve. The rampant nature by which cancer invades local and distant tissues, as well its apparent ability to spread between related individuals led some, such as Peyton Rous in 1910, to suggest that cancer was an infectious condition. He was awarded a Nobel Prize in 1966 for the 50 years of work into investigating a link between sarcoma in chickens and a retrovirus that became known as Rous sarcoma virus. He had shown how retroviruses are able to integrate sequences of DNA coding for errors in cellular replication control (oncogenes) by introducing into the human cell viral RNA together with a reverse transcriptase. Viruses are now implicated in many cancers, and in countries where viruses such as HIV and EBV are endemic, the high incidence of malignancies such as Kaposi’s sarcoma and Burkitt’s lymphoma is likely to be directly related. There are several families of viruses associated with cancer, broadly classed into DNA viruses, which mutate human genes using their own DNA, and retroviruses, like Rous sarcoma virus, which insert viral RNA into the cell, where it is then transcribed into genes. This link with viruses has not only led to an understanding that cancer originates from genetic mutations, but has also become a key focus in the design of new anticancer therapies. Traditional chemotherapies either alter DNA structure (as with cisplatin) or inhibit production of its component parts (as with 5-fluorouracil.) These broad-spectrum agents have many and varied side effects, largely due to their non-specific activity on replicating DNA throughout the body, not just in tumour cells. New vaccine therapies utilizing gene-coding viruses aim to restore deficient biological pathways or inhibit mutated ones specific to tumour cells. The hope is that these gene therapies will be effective and easily tolerated by patients, but development is currently progressing with caution. In a trial in France of ten children suffering from X-linked severe combined immunodeficiency and who were injected with a vector that coded for the gene product they lacked, two of the children subsequently died from leukaemia. Further analysis confirmed that the DNA from the viral vector had become integrated into an existing, but normally inactive, proto-oncogene, LM02, triggering its conversion into an active oncogene, and the development of life-threatening malignancy. To understand how a tiny change in genetic structure could lead to such tragic consequences, we need to understand the molecular biology of the cell and, in particular, to pay attention to the pathways of growth regulation that are necessary in all mammalian cell populations. Errors in six key regulatory pathways are known as the ‘hallmarks of cancer’ and will be discussed in the rest of this chapter.

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Books on the topic 'Mammalian tissues'

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